The basic mechanical determinants of myocardial oxygen consumption (MVO2) are well described, but the way that changing mechanical conditions during a contraction interact with myocardial metabolism to result in the differing net MVO2 of various types of auxotonic contraction is less certain. For example, it is known descriptively that tension generation is a more important mechanical determinant of MVO2 than shortening, but the interaction throughout a contraction of tension and length changes with MVO2 is poorly understood. In the initial portion of this investigation it was found that during myocardial tetanus, when activation is maximum and constant, the mechanical determinants of MVO2 which apply during twitch contractions are no longer important. Instead, MVO2 relates very closely to the duration of contraction and is very little modified by the associated mechanical conditions. The difference between this finding and the fact that nechanical conditions are very important in determining MVO2 during twitch contractions has led to the hypothesis to be examined in the proposed investigation: the basis for the mechanical determinants of MVO2 during normal auxotonic twitch contractions is a dynamic interaction between MVO2 and mechanical state. That is, the rate and time course of oxygen requiring actin-myosin interactions during a twitch contraction are modulated during that contraction by its ongoing mechanical result. This hypothesis will be tested by defining in a polarographic myograph the oxygen consumption sampled incrementally throughout twitch contractions of isolated heart muscle in the two mechanical situations where the greatest difference in MVO2 is usually observed: (1) lightly preloaded isotonic contractions and (2) isometric contractions at the optimum length for tension generation. This measurement of cumulative MVO2 at known increments of twitch duration will allow the interaction of active tension and shortening with MVO2 to be studied throughout these two types of contraction and define any potential feedback between mechanical state and myocardial energetics.